Evidence map›Paper›PMID 28377355›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2017

[Role of Beclin 1 gene in autophagy and apoptosis of SW620 cells].

Meng Lv, Hang Lu

Abstract read
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Meng LvGraduate School, First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121000, China.E-mail: 122081148@qq.com.
Hang Lu
Affiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo study the role of Beclin1 gene in autophagy and apoptosis of SW620 cells.

methodsRNA interference was used to knockdown the expression of Beclin 1 in SW620 cells, and the cell viability was measured by MTT assays. The autophagic activity in serum-starved SW620 CRC cells was evaluated by assessing endogenous microtubule-associated protein 1 light chain 3 (LC3) protein levels using immunofluorescence assay. Flow cytometry was used to measure the apoptosis rate of SW620 cells treated with serum deprivation, staurosporine or etoposide, and the protein expression of Beclin1 was detected using Western blotting.

resultsThe viability of cells in pSUPER-Becl group was significantly reduced after serum deprivation (P<0.05). Serum deprivation for 24 h resulted in a stronger apoptotic resistance in cells in the control and pSUPER-non groups than in pSUPER-Becl group (P<0.05). Treatment with staurosporine the most significantly increased the cell apoptosis in pSUPER-Becl group (P<0.05), and similar effect was observed with etoposide treatment (P<0.05). As the time of serum deprivation extended, the expression of Beclin 1 in control group and pSUPER-non group increased progressively (P<0.05), which was consistent with the changes in LC3 expression; LC3 expression in pSUPER-Becl group decreased significantly with a prolonged serum starvation (P<0.05).

conclusionBeclin 1 is a crucial regulator of autophagy and apoptosis in colorectal cancer cells to maintain the balance between autophagy and apoptosis. Beclin 1 may serve as a protective mechanism to protect colorectal cancer cells from injury caused by low nutrition and chemotherapy byregulating cell autophagy.

Indexed as

ApoptosisAutophagyBeclin-1Cell Line, TumorHumansMicrotubule-Associated ProteinsBeclin-1BECN1 protein, humanMAP1LC3A protein, humanMicrotubule-Associated Proteins

Identifiers

PMID28377355
PMCPMC6780449
OpenAlexW3024671991

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.